Category Archives: Endocrinology (diabetes)

– Type 1 and type 2 diabetes.
– Diabetes causes and symptoms.
– How blood glucose is regulated?

Intermittent Fasting – How It Works? with Animation

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Intermittent fasting refers to eating plans that alternate between fasting and eating periods. The goal is to systematically starve the body long enough to trigger fat burning. While research is still underway and the method may not be suitable for everyone, there is evidence that, when done correctly, intermittent fasting can help lose weight, lower blood pressure and cholesterol, prevent or control diabetes, and improve brain’s health.

During a meal, carbohydrates in food are broken down into glucose. Glucose absorbs through the intestinal wall into the bloodstream and is transported to various organs, where it serves as the major energy source. Excess glucose is stored for later use in the liver and adipose tissue, in the form of glycogen and fats.  In between meals, when the body is in the fasted state, the liver converts glycogen back to glucose to keep supplying the body with energy. Typically, an inactive person takes about 10 to 12 hours to use up the glycogen stores, although someone who exercises may do so in much less time. Once the reserve of glycogen in the liver is depleted, the body taps into energy stores in adipose tissues. This is when fats are broken down into free fatty acids which are then converted into additional metabolic fuel in the liver. Thus, if the fasted state lasts long enough, the body burns fat for energy and loses that extra fat. Losing the extra fat is translated into a range of associated health benefits.

Insulin is the hormone required for driving glucose into cells. Insulin level is regulated to match the amount of glucose in the blood, that is, high after a meal and low between meals. Because insulin is secreted after each meal, eating throughout the day keeps insulin levels high most of the time. Constant high insulin levels may de-sensitize body tissues, causing insulin insensitivity – the hallmark of prediabetes and diabetes type 2. Fasting helps keep insulin levels low, reducing diabetes risks.

Fasting also has beneficial effect on the brain. It challenges the brain the same way physical or cognitive exercise does. It promotes production of neurotrophic factors, which support the growth and survival of neurons.

Fasting, however, is not for everyone. Among those who should not attempt fasting are:

– children and teens

– pregnant or breastfeeding women

– people with eating disorders, diabetes type 1, advanced diabetes, or some other medical problems

– people who are underweight or frail

Fasting can also be unsafe if overdone, or if not done correctly.

There are several approaches to intermittent fasting, but the easiest to achieve is perhaps the one that simply extends the usual nighttime fast. A daily cycle of 16-hour fast followed by a 8-hour eating window is usually sustainable.

For intermittent fasting to be safe and effective, it must be combined with balanced meals that provide good nutrition. It is important to stay hydrated, and know your physical limits while fasting. The fast must be broken slowly. Overeating after fast, especially of unhealthy foods, must be avoided.

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Gestational diabetes, with Animation

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Gestational diabetes is a transient form of diabetes mellitus some women may acquire during pregnancy. Diabetes refers to high levels of blood glucose, commonly known as blood sugar. Glucose is the major energy source of the body. It comes from digestion of carbohydrates and is carried by the bloodstream to the body’s cells. But glucose cannot enter the cells on its own; to do so, it requires assistance from a hormone produced by the pancreas called insulin. Insulin induces the cells to take up glucose, thereby removing it from the blood. Diabetes happens when insulin is either deficient or not used effectively. Without insulin, glucose cannot enter the cells; it stays in the blood, causing high blood sugar levels.
During pregnancy, a temporary organ develops to connect the mother and the fetus, called the placenta. The placenta supplies the fetus with nutrients and oxygen, as well as produces a number of hormones that work to maintain pregnancy. Some of these hormones impair the action of insulin, making it less effective. This insulin-counteracting effect usually begins at about 20 to 24 weeks of pregnancy. The effect intensifies as the placenta grows larger, and becomes most prominent in the last couple of months. Usually, the pancreas is able to adjust by producing more insulin, but in some cases, the amount of placental hormones may become too overwhelming for the pancreas to compensate, and gestational diabetes results.
Any woman can develop gestational diabetes, but those who are overweight or have family or personal history of diabetes or prediabetes are at higher risks. Other risk factors include age, race, and having previously given birth to large babies.
While gestational diabetes usually resolves on its own after delivery, complications may arise if the condition is severe and/or poorly managed.
Because of the constant high glucose levels in the mother’s blood, the fetus may receive too much nutrients and grow too large, complicating the birth process, and a C-section may be needed for delivery.
High levels of glucose also stimulate the baby’s pancreas to produce more insulin than usual. Shortly after delivery, as the baby continues to have high insulin levels but no longer receives sugar from the mother, the baby’s blood sugar levels can drop suddenly and become exceedingly low, causing seizures. The newborn’s blood sugar level must therefore be monitored and corrected with prompt feeding, or if necessary, with intravenous glucose.
High blood sugar may also increase the mother’s blood pressure and risks of preterm birth. Future diabetes in both mother and child is also more likely to occur.
Gestational diabetes can be successfully managed, or even prevented, with healthy diets, physical exercise, and by keeping a healthy weight before and during pregnancy. In some cases, however, medication or insulin injection may be needed.

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What is A1C? Explained with Animation

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A1C test is a blood test used to diagnose diabetes and monitor the progress of a treatment plan. The test result reflects the average blood sugar levels in the past 3 months.
A1C is a type of glycated hemoglobin – a hemoglobin that is bound to glucose. Hemoglobin is the major protein of red blood cells. A1C forms as a result of interaction between red blood cells and sugar in the blood. The higher the blood glucose levels, the more glucose binds to hemoglobin, the greater the amount of A1C. The A1C blood test reports the percentage of hemoglobin that is bound to glucose.
Once a hemoglobin is glycated, it remains that way in the blood, until the red blood cell carrying it is removed from the circulation. Because the average lifespan of a red blood cell is 3 to 4 months, A1C measurement represents the status of blood glucose for the past 3 months or so.
A normal blood glucose level corresponds to an A1C result of less than 5.7%. An A1C level higher than 6.5% indicates diabetes. Between 5.7 and 6.5% is prediabetes.
An estimated average glucose level, eAG, measured in concentration units, milligrams per deciliter or millimoles per liter, can be calculated and often reported in addition to the A1C percentage. eAG helps patients link A1C to the numbers they obtain at home using a blood sugar measuring device.
A1C is an important tool for managing diabetes. For most diabetics, the goal is to bring A1C level down to 7% or less. However, patient’s age and other health conditions must be taken into account when setting goals. In general, younger patients who don’t often experience severe low glucose, known as hypoglycemia, need lower goals to avoid diabetes complications in the many years ahead. Older patients or those having frequent low-glucose episodes, may have a higher goal.
When A1C can NOT be used?

It is important to note that several factors can affect the accuracy of A1C test result, in which case, unless corrections can be made, A1C cannot be used to assess blood glucose levels. For example, people with blood disorders such as sickle cell disease, thalassemia, or hemolytic anemia may have a lower than expected A1C because their red blood cells have a shorter lifespan. Iron deficiency anemia, on the other hand, is associated with increased red blood cell lifespan and falsely high A1C measurements. Some people of African, Mediterranean, or Southeast Asian descent may have uncommon forms of hemoglobin that produce falsely high or low results. Certain kidney and liver diseases may affect the turnover rate of red blood cells and give rise to inaccurate A1C readings. Finally, recent blood loss or transfusion will also skew the test results.

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Water and Sodium Balance, Hyper- and Hyponatremia

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A human body contains 50 to 70% water, of which about 2 thirds is located inside the cells, the other one third is in the extracellular fluid and blood plasma. Water can move freely between different compartments in the body, but its direction is determined by which compartment has more solutes, or higher osmolality. As a rule, water moves from the more diluted solution to the more concentrated solution – from lower to higher osmolality.
Sodium, being the major extracellular solute, is the principal determinant of plasma osmolality and the most important regulator of fluid balance. A normal blood sodium level is kept between 135 and 145 mmol/L. Hyponatremia occurs when blood sodium falls below 135, while hypernatremia is when it exceeds 145.
Clinical manifestations of sodium disorders reflect disturbances in water movement in the most sensitive organ of the body – the brain. In hypernatremia, high blood sodium levels draw water out of the brain cells, causing dehydration and shrinkage. Whereas in hyponatremia, low concentrations of plasma sodium drive water into brain cells, making them swell, causing edema. Both situations produce neurologic symptoms, which can range from headache, confusion, to seizures, coma or even death.
Hypernatremia most often occurs because of inadequate water intake, or excessive water loss or excretion. Water intake is regulated by thirst. When a decreased body fluid volume or an increased plasma osmolality is detected, the brain perceives it as thirst and produces water-seeking behavior. Impaired thirst mechanism is a common cause of hypernatremia in the elderly.
The body loses water primarily by excreting it in urine. Water excretion by the kidneys is mainly regulated by vasopressin, a hypothalamic hormone that causes the kidneys to retain water in response to low blood volume or high plasma osmolality. Impaired vasopressin release, renal dysfunction, and use of certain diuretics, are common causes of excessive water loss through the kidneys.
Fluid loss through the digestive tract is normally negligible, but can be substantial in vomiting or diarrhea. Sweat loss though skin can be significant in extreme heat or during excessive exercise.
Chronic hypernatremia is treated with oral hypotonic fluids, while acute or severe hypernatremia may require intravenous administration along with constant monitoring to avoid overcorrection. The underlying cause must also be addressed.
For hyponatremia, treatment depends on the body fluid volume:
– In low volume, or hypovolemic hyponatremia, both sodium and water levels decrease, but sodium loss is relatively greater. This commonly occurs due to loss of sodium-containing fluids, as in vomiting and diarrhea, especially when loses are replaced with plain water. This type is managed by rehydration with isotonic fluids.
– In high volume, or hypervolemic hyponatremia, both sodium and water levels increase, with a relatively greater increase in body water. This often results from fluid retention in conditions such as heart failure, liver cirrhosis, or kidney failure; and is usually treated with diuresis.
– In normal volume, or euvolemic hyponatremia, sodium level is normal, but there is an increase in total body water. This can be caused by excessive water intake combined with renal insufficiency, or syndrome of inappropriate ADH secretion, which causes the kidneys to retain more water. This type is managed by restricting free water intake and addressing the underlying cause.
Premenopausal women are more susceptible to acute hyponatremia with severe brain edema, perhaps because female hormones increase vasopressin level, and inhibit the brain sodium-potassium pump, which pumps sodium out of the cell and helps maintain normal brain volume.
Acute or symptomatic hyponatremia is an emergency and should be treated with intravenous hypertonic sodium chloride, but sodium levels must be closely monitored to avoid overly rapid correction.

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The Endocrine System, Overview with Animation

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The endocrine system is one of the two systems that are responsible for communication and integration between various body tissues, the other being the nervous system. Endocrine communication is achieved by means of chemical messengers called hormones. Hormones are produced in endocrine glands and secreted into the bloodstream to reach body tissues. A hormone can travel wherever the blood goes, but it can only affect cells that have receptors for it. These are called target cells. There are 2 major types of hormones: steroid hormones derived from cholesterol and are lipid-soluble; and non-steroid hormones derived from peptides or amino-acids and are water-soluble. Lipid-soluble steroid hormones can cross the cell membrane to bind to their receptors inside the cell, either in the cytoplasm or nucleus. Steroid hormone receptors are typically transcription factors. Upon forming, the hormone/receptor complex binds to specific DNA sequences to regulate gene expression, and thus mediating cellular response. On the other hand, water-soluble non-steroid hormones are unable to cross the lipid membrane and therefore must bind to receptors located on the surface of the cell. The binding triggers a cascade of events that leads to production of cAMP, a second messenger that is responsible for cellular response to hormone. It does so by changing enzyme activity or ion channel permeability.
Major endocrine glands include: the hypothalamus, pituitary gland, pineal gland, thyroid and parathyroid glands, thymus, adrenal gland, islets of the pancreas, and testes in men or ovaries in women. The endocrine system also includes hormone-secreting cells from other organs such as kidneys and intestine.
Except for the hypothalamus and the pituitary, different endocrine glands are involved in different, more or less independent, processes. For example, the pancreas produces insulin and glucagon that keep blood sugar levels in check; the parathyroid glands produce hormones that regulate calcium and phosphorus; thyroid hormones control metabolic rates; while the ovaries and testes are involved in reproductive functions. On the other hand, the hypothalamus and pituitary gland play a more central, integrative role. The hypothalamus is also part of the brain. It secretes several hormones, called neuro-hormones, which control the production of other hormones by the pituitary. Thus, the hypothalamus links the nervous system to the endocrine system. The pituitary is known as the master gland because it controls the functions of many other endocrine glands. (See “Hypothalamus and Pituitary Gland video for details!)
A major role of the endocrine system is to maintain the body’s stable internal conditions, or homeostasis, such as blood sugar levels or serum calcium levels. To do this, it utilizes negative feedback mechanisms, which work very much like a thermostat: the heater is on when the temperature is low, off when it’s high. For example, when blood glucose level is high, such as after a meal, glucose induces insulin release from the pancreas. Insulin helps body cells consume glucose, clearing it from the blood. Low blood glucose can no longer act on the pancreas, which now stops releasing insulin. Another example is the regulation of thyroid hormones levels which are induced by a pituitary hormone called thyroid-stimulating hormone, TSH. TSH, in turn, is under control of thyrotropin-releasing hormone, TRH, from the hypothalamus. When thyroid hormone levels are too high, they suppress the secretion of TSH and TRH, consequently inhibiting their own production.

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How obesity and physical inactivity cause prediabetes and diabetes

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Diabetes refers to a group of conditions characterized by high levels of blood glucose, commonly known as blood sugar. Glucose comes from digestion of carbohydrates in food, and is carried by the bloodstream to various body tissues. But glucose cannot cross the cell membrane to enter the cells on its own; to do so, it requires assistance from a hormone produced by the pancreas called insulin. Binding of insulin to its receptor on a target cell triggers a signaling cascade that brings glucose transporters to the cell membrane, creating passageways for glucose to enter the cells. In most tissues, muscles for example, glucose is used as an energy source, while in the liver and adipose tissue, it is also stored for later use, in the form of glycogen and fats.  When the body is in the fasted state, the liver produces and secretes glucose into the blood, while adipose tissues release free fatty acids to the liver where they are converted into additional metabolic fuel.

Diabetes happens when insulin is either deficient or its action is compromised. Without insulin, glucose cannot enter the cells; it stays in the blood, causing high blood sugar levels.

There are 2 major types of diabetes. Type 1 is when the pancreas does not produce enough insulin; and type 2 is when the body’s cells do not respond well to insulin – they are insulin-resistant. Both types are caused by a combination of genetic and environmental factors but genetics plays a major role in type 1, while lifestyle is a predominant risk factor for type 2. For this reason, type 1 diabetes usually starts suddenly in childhood, while type 2 progresses gradually during adulthood, going through a so called pre-diabetic stage, which is defined as borderline blood sugar levels: higher than normal, but lower than diabetic. Pre-diabetes is very common, and while not always developing into full-blown diabetes, over time, it can cause much the same damage to the body. Unhealthy lifestyle is the trigger of pre-diabetes and the main driving force behind its progression to diabetes type 2. The key factors are obesity and physical inactivity.

There are at least 2 ways by which obesity can cause insulin resistance and high blood glucose.

First, in obesity, fat cells have to process more nutrients than they can manage and become stressed. As a result, they release inflammatory mediators, known as cytokines. Cytokines interfere with the signaling cascade by insulin receptor, blocking the action of insulin, thereby causing the cells to become less responsive to insulin.

Second, excess adipose tissue releases abnormally large amount of free fatty acids to the liver – an event that normally happens only when the body is fasting. This tricks the liver into producing and releasing more glucose into the blood. High blood glucose stimulates further insulin secretion. Constant high insulin levels de-sensitize body tissues, causing insulin insensitivity.

Intra-abdominal fat appears to produce more fatty acids and cytokines, and therefore has more severe effect on blood glucose, than subcutaneous, or peripheral fat. For this reason, large waist size is a greater risk factor than high body mass index.

Sedentary lifestyle, apart from having indirect effect by causing weight gain, has its own direct impact on insulin resistance. This is because physical activity is required to maintain healthy blood sugar levels. Physical activity increases energy demand by the muscles, which consume glucose from the blood, and subsequently from glucose storage in the liver and adipose tissue. High energy expenditure helps to clear up faster the spikes of blood glucose that follow every meal. High energy demand also promotes better cellular response to insulin, increasing insulin sensitivity. Studies have shown that physical inactivity, even for a short period of time, results in consistently higher spikes of blood sugar after meals, which can trigger pre-diabetic changes in healthy individuals, or speed up transition from pre-diabetes to diabetes. More importantly, this happens not only to over-weight patients, but also to people with seemingly healthy weight. This is probably because inactivity reduces muscle mass and replaces it with adipose tissue, thus having serious effects on blood sugar levels while still maintaining an overall normal weight.

The bottom line is, in order to prevent diabetes, weight management must be combined with physical activity or exercise.

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Amenorrhea, Pathology and Causes, with Animation

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Amenorrhea is the ABSENCE of menstrual periods in a woman of reproductive age. Absence of menses is normal in pregnant, breastfeeding and menopausal women, but pathological otherwise. Amenorrhea is not a disease on its own, but rather a symptom of a variety of underlying conditions. PRIMARY amenorrhea is when a woman has NEVER had her periods, while SECONDARY amenorrhea is when a woman has STOPPED having them.

Menstruation is part of the menstrual cycle, the monthly events that occur within a woman’s body in preparation for the possibility of pregnancy. Each month, an egg is released from an ovary in a process called ovulation. At the same time, the lining of the uterus THICKENS, ready for pregnancy. If fertilization does NOT take place, the lining of the uterus is shed in menstrual bleeding and the cycle starts over. The menstrual cycle is under control of multiple hormones secreted by the hypothalamus, pituitary gland, and ovaries. Basically, the hypothalamus produces gonadotropin-releasing hormone, GnRH; the anterior pituitary secretes follicle-stimulating hormone, FSH, and luteinizing hormone, LH; while the ovaries produce estrogen and progesterone. These hormones are involved in a REGULATORY network that results in monthly cyclic changes responsible for follicular maturation and ovulation.

Amenorrhea can be caused by ANATOMICAL or ENDOCRINE problems.

Anatomical causes refer to abnormalities in the female reproductive system and include:

– absent or underdeveloped female organs in some genetic disorders, such as MRKH syndrome

– congenital defects that OBSTRUCT blood outflow

– and destruction of the uterine cavity by previous infections or surgeries.

Endocrine problems refer to structural or functional defects of the hypothalamus, pituitary gland and ovaries. A common cause in this category is the impaired function of the hypothalamus which occurs when the hypothalamic-pituitary-ovarian axis is SUPPRESSED due to an ENERGY DEFICIT. This can result from weight loss, eating disorders, excessive exercise, malabsorption syndromes, or emotional stress. The common feature is a REDUCED production of GnRH by the hypothalamus, which results in corresponding LOW levels of FSH and LH and subsequent impairment of follicular maturation and absence of ovulation.

Other endocrine causes include:

– Kallmann’s syndrome, a genetic disorder associated with congenital defects of the hypothalamus, causing GnRH deficiency.

– Sheehan’s syndrome, a condition in which excessive blood loss during childbirth or chronic hypotension during pregnancy IMPAIRS PITUITARY functions.

– Tumors, infections, trauma or autoimmune destruction of the pituitary gland.

– Polycystic ovary syndrome, an endocrine disorder in which FSH deficiency disrupts follicle maturation.

– Loss of normal ovarian function in conditions such as Turner’s syndrome

– Thyroid disorders

Treatment is by addressing the underlying cause and can range from nutrition plans, hormonal therapy to surgical interventions.

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Polycystic Ovary Syndrome, with animation

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Polycystic Ovary Syndrome: Diagnosis, Causes, Pathology, Treatment

Polycystic ovary syndrome, or PCOS, is a common HORMONAL disorder affecting about 10% of all women of reproductive age. PCOS is diagnosed when AT LEAST 2 of the following symptoms are present:

  • irregular periods due to MISSED ovulation.
  • excess male hormone (androgen) as evidenced by lab tests or physical signs, such as excess facial and body hair, severe acne, and baldness.
  • presence of numerous small fluid-filled cysts in the ovaries which can be seen as dark circles on an ultrasound image. This is the symptom that originally gave the condition its name but is NOT always present in PCOS patients.

PCOS is highly heritable, but the inheritance pattern is complex, with multiple genetic factors implicated in the susceptibility to the disease. While the exact cause of PCOS is unknown, disturbances in a number of hormones are thought to be responsible. PCOS patients usually have EXCESS luteinizing hormone, LH, together with a relatively LOW level of follicle-stimulating hormone, FSH, and increased levels of insulin.

An ovary contains hundreds of thousands of IMMATURE eggs, each of these is enclosed in a structure called a follicle. Each month, a number of these follicles develop, compete with each other; and one of them survives and gives rise to a MATURE egg that is released during ovulation. Follicle development is mediated by FSH, a pituitary hormone. In PCOS patients, FSH deficiency results in ARREST of follicular maturation: the follicles stop halfway through their development and become cysts. IMPAIRED follicular development means NO mature egg produced or released, hence the ABSENCE of ovulation.

Insulin is a hormone produced by the pancreas and is necessary for consumption of blood glucose by the body’s cells. INcreased insulin level in PCOS patients is a result of the body compensatory response to insulin RESISTANCE associated with PCOS. Excess insulin, together with high levels of luteinizing hormone, induce and maintain OVERproduction of androgen by the ovaries.

Common complications of PCOS include: infertility, miscarriage or premature birth, type 2 diabetes, obesity, cardiovascular diseases, mood disorders, and endometrial cancer.

While the choice of treatment may depend on the patient’s individual concerns, treating insulin resistance is generally recommended for all women with PCOS. Life style changes such as exercise, dieting and weight loss, and medications such as metformin, can LOWER both insulin and androgen levels, thus reducing the risks of type 2 diabetes, and improving ovulation. Patients who want to get pregnant may also be prescribed anti-estrogen medications such as clomiphene.  On the other hand, when fertility is not the goal of treatment, hormonal birth control, a combination of estrogen and progestin, is usually prescribed to regulate the menstrual cycle and reduce risks of endometrial cancer. This treatment may also help improve acne and reduce extra body hair.

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Hypocalcemia: Causes, Symptoms, Pathology, with Animation

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Dietary calcium enters the blood through the small intestine and exits in urine via the kidneys. In the body, most calcium is located in bones, only about 1% is in the blood and extracellular fluid. There is a continual exchange of calcium between blood serum and bone tissue.

The amount of calcium in circulation is MAINLY regulated by 2 hormones: parathyroid hormone, PTH, and calcitriol. PTH is produced in the parathyroid gland while calcitriol is made in the kidney. When serum calcium level is low, PTH is UPregulated. PTH acts to PROMOTE calcium release from bones and REDUCE calcium loss from urine. At the same time, it stimulates production of calcitriol, which promotes absorption of calcium in the small intestine while also INcreases RE-absorption in the kidney. Together, they bring UP calcium levels back to normal. The REVERSE happens when calcium level is high. This feedback loop keeps serum calcium concentrations within the normal range.

Hypocalcemia refers to abnormally LOW levels of calcium in the blood and is generally defined as serum calcium level LOWER than 2.1 mmol/L. Because the total serum calcium includes albumin-bound and free-ionized calcium, of which only the LATTER is physiologically active, calcium levels must be corrected to account for albumin changes. For example, decreased albumin levels, such as in liver diseases, nephrotic syndrome, or malnutrition, produce LOWER serum calcium values but the amount of FREE calcium may STILL be normal. On the other hand, in conditions with high blood pH, albumin binds MORE calcium; leaving LESS FREE-ionized calcium in the serum while the total calcium level may appear normal.

The most common cause of hypocalcemia is PTH deficiency resulting from DEcreased function of the parathyroid glands, or hypoparathyroidism.  Hypoparathyroidism, in turn, may be caused by a variety of diseases and factors. These include:

– accidental removal or damage of the parathyroid glands during a surgery

– autoimmune disorders

– congenital disorders: mutations that set the “normal calcium levels” to a lower value

– other genetic disorders that produce underdeveloped or non-functional parathyroid glands

– magnesium deficiency

Other causes of hypocalcemia include low vitamin D intake/production, and excessive loss of calcium from the circulation such as in kidney diseases, tissue injuries or gastrointestinal diseases.

While chronic moderate hypocalcemia may be asymptomatic, ACUTE and severe hypocalcemia can be life-threatening. Most symptoms of acute hypocalcemia can be attributed to the effect it has on action potential generation in neurons. Because extracellular calcium INHIBITS sodium channels, and consequently depolarization, REDUCED calcium level makes it EASIER for depolarization to occur. Hypocalcemia therefore INCREASES neuronal excitability, causing neuromuscular irritability and muscle spasms.  Early symptoms often include numbness and tingling sensations around the mouth, in the fingers and toes. As the disease progresses, muscle spasms may manifest as tetany, wheezing, voice change, and dysphagia. Seizures may occur in severe cases. Effects of hypocalcemia on cardiac function include long QT interval due to prolonged ST fragment, congestive heart failure and hypotension.

Acute hypocalcemia should be treated promptly with intravenous calcium. Chronic hypocalcemia is usually treated with oral calcium and possibly vitamin D supplementation.

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Hypercalcemia: Calcium metabolism, Hormonal control, Etiology, Diagnosis, Symptoms, Treatment and Prognosis, with Animation

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Hypercalcemia refers to abnormally HIGH levels of calcium in the blood.
Dietary calcium enters the blood through the small intestine and exits in urine via the kidneys. In the body, most calcium is located in bones, only about 1% is in the blood and extracellular fluid. There is a continual exchange of calcium between blood serum and bone tissue.
The amount of calcium in circulation is MAINLY regulated by 2 hormones: parathyroid hormone (PTH) and calcitriol. PTH is produced in the parathyroid gland while calcitriol is made in the kidney. When serum calcium level is low, PTH is UP-regulated. PTH acts to PROMOTE calcium release from bones and REDUCE calcium loss from urine. At the same time, it stimulates production of calcitriol, which promotes absorption of calcium in the small intestine while also INcreases RE-absorption in the kidney. Together, they bring UP calcium levels back to normal. The REVERSE happens when calcium level is high. This feedback loop keeps serum calcium concentrations within the normal range.
Hypercalcemia is generally defined as serum calcium level GREATER than 2.6 mmol/L. Because the total serum calcium includes albumin-bound and free-ionized calcium, of which only the LATTER is physiologically active, calcium levels must be corrected to account for albumin changes. For example, INcreased albumin levels produce HIGHER serum calcium values but the amount of FREE calcium may STILL be normal. On the other hand, in conditions with low blood pH, albumin binds LESS calcium; releasing MORE FREE calcium while the total serum calcium may appear normal.
Most symptoms of hypercalcemia can be attributed to the effect it has on action potential generation in neurons. High levels of extracellular calcium INHIBIT sodium channels, which are essential for DEpolarization. Hypercalcemia therefore REDUCES neuronal excitability, causing confusion, lethargy, muscle weakness and constipation. In most cases, excess calcium in the blood is a direct result of calcium release from bones as they break down, becoming weak and painful. As the kidneys try to get rid of the extra calcium, MORE water is also removed, resulting in dehydration, excessive thirst and kidney stones. Extremely high extracellular calcium may also affect cardiac action potentials, causing arrhythmias. Typical ECG findings include short QT interval, and in severe cases, presence of Osborn waves.
While hypercalcemia may result from a variety of diseases and factors, hyperparathyroidism and cancers are responsible for about 90% of cases, with the former being by far the most common cause. In HYPERparathyroidism, PTH is OVERproduced due to benign or malignant growths within the parathyroid gland.
An existing cancer elsewhere in the body can cause hypercalcemia in 2 major ways. First, some cancer cells produce a protein similar to PTH, called PTHrP, which acts like PTH to increase serum calcium. Unlike PTH, however, PTHrP is NOT subject to negative feedback; consequently, calcium levels may keep rising unchecked. Second, cancers may spread to bone tissues, causing bone resorption or osteolysis, and subsequent calcium release into the blood.
Hypercalcemia treatment consists of lowering blood calcium levels with a variety of drugs, and addressing the underlying cause. While treatment outcome for hyperparathyroidism is generally excellent, prognosis for malignancy-related hypercalcemia is poor, possibly because it usually occurs in later stages of cancer.

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